Background: Advances in neonatal cardiac care have improved survival in infants with congenital heart disease (CHD), shifting clinical attention toward early neurological morbidity. While cardiac anatomical complexity has traditionally been considered a major determinant of brain injury, emerging evidence suggests that genetic and systemic factors may play a more important role. Transfontanellar ultrasound (TFUS) is widely used as a bedside screening tool for early detection of neonatal brain abnormalities. Aim: To assess the incidence of abnormal TFUS findings in neonates with CHD and identify clinical and genetic predictors of early neurological vulnerability independent of cardiac anatomy. Materials and Methods: We conducted an observational cohort study including 138 neonates with CHD who underwent TFUS evaluation at a tertiary care center in Iași, Romania. Demographic, perinatal, clinical, genetic, and therapeutic data were collected retrospectively. CHD complexity was classified using the Bethesda classification. Univariate and multivariate logistic regression analyses were performed to identify predictors of abnormal TFUS findings. Results: Abnormal TFUS findings were identified in 42 neonates (30.4%), most commonly ventricular dilatation, intracranial hemorrhage, and choroid plexus cysts. In multivariate analysis, positive genetic testing was the strongest independent predictor (OR 3.9, 95% CI 1.5–10.2), followed by mechanical ventilation dependence (OR 2.7, 95% CI 1.1–6.5) and high Bethesda risk category (OR 2.2, 95% CI 1.0–4.8). Cardiac anatomical classification and gestational age were not independently associated with abnormal TFUS findings. Conclusions: In neonates with CHD, early TFUS abnormalities appear to be driven mainly by genetic and systemic factors rather than cardiac anatomy alone, supporting integrative risk stratification approaches for targeted neurological surveillance.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a distinct and potentially curable form of pulmonary hypertension that develops following incomplete resolution of acute pulmonary embolism, leading to persistent fibrotic obstruction of the pulmonary arteries and progressive microvascular disease. Although CTEPH has traditionally been assessed using steady-flow hemodynamic parameters such as mean pulmonary arterial pressure and pulmonary vascular resistance, growing evidence suggests that pulmonary artery stiffness and altered vascular biomechanics are critical contributors to disease severity, right ventricular dysfunction, and patient outcomes. This narrative review summarizes current knowledge on the structural remodeling and biomechanical behavior of pulmonary arteries in CTEPH, with emphasis on changes affecting arterial compliance, impedance, and right ventricle–pulmonary artery coupling. Key mechanisms include thrombus organization, endothelial dysfunction, smooth muscle cell proliferation, extracellular matrix deposition, and mechanobiological feedback loops that reinforce vascular stiffening. The review further discusses available experimental and computational approaches used to characterize pulmonary vascular mechanics and highlights the clinical relevance of biomechanical markers in improving prognostic stratification and therapeutic decision-making. Finally, it outlines gaps in current evidence regarding reversibility of vascular stiffness and the long-term impact of surgical, interventional, and medical therapies, supporting the need for integrated biomechanical assessment in future CTEPH research and management.

Background: Pulmonary embolism (PE) is a major cause of cardiovascular death and was increasingly diagnosed during and after the COVID-19 pandemic, highlighting the role of inflammation alongside genetic and acquired risk factors. Despite effective therapies, PE remains underdiagnosed. This study analyzed patient characteristics, risk factors, inflammatory markers, and management strategies. Materials and Methods: We conducted a retrospective study of 97 patients with PE admitted to the Cardiology Department of the County Emergency Clinical Hospital Brașov between March 2021 and April 2022. Clinical, biological, and therapeutic data were systematically evaluated. Results: The mean age was 66.8 years, with near-equal sex distribution. The most frequent symptoms were dyspnea, unilateral lower limb edema, and chest pain; hemodynamic instability was rare. Major risk factors included age >60 years, hypertension, and obesity. One-third of patients had recent SARS-CoV-2 infection or vaccination (<4 months). Inflammatory and thrombotic markers (leukocytosis, CRP, fibrinogen, D-dimer) were frequently abnormal. Most patients received low-molecularweight heparin; thrombolysis was used selectively. Conclusions: PE management during the pandemic emphasized the importance of inflammation in risk stratification, monitoring, and prognosis. Identifying patient-specific risk factors and refining treatment strategies remain essential for improving outcomes in this high-risk population.

Background: Acute coronary syndrome (ACS) includes ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI), each with distinct clinical profiles and outcomes. While STEMI is typically associated with more extensive infarcts, emerging data suggest NSTEMI may carry a greater burden of comorbidities and anatomical complexity. Objective: To compare the incidence of ventricular arrhythmias and hemodynamic instability in patients with STEMI vs. NSTEMI and to analyze the distribution of culprit coronary lesions. Methods: This retrospective single-center study included 172 patients who underwent coronary revascularization between April and July 2021. Clinical outcomes, arrhythmias, and hemodynamic instability were compared between groups with STEMI (n = 108) and NSTEMI (n = 64). Culprit lesions were evaluated by angiography and categorized by vessel. Results: Hemodynamic instability was significantly more common in patients with NSTEMI (10.93%) compared to STEMI (0.18%) (p = 0.005). Ventricular arrhythmias occurred in 12.03% of patients with STEMI and 7.81% of patients with NSTEMI, with no significant difference. Left main coronary artery lesions were notably more frequent in NSTEMI (47.4% vs. 2.04%; p < 0.0001), whereas right coronary artery involvement was higher in STEMI (40.81% vs. 7.4%; p < 0.0001). Ventricular arrhythmias were significantly associated with circumflex artery lesions in patients with NSTEMI (p = 0.0001). Conclusions: Despite often being perceived as lower risk, patients with NSTEMI exhibited a higher rate of hemodynamic instability and more complex coronary involvement, particularly left main disease. These findings highlight the need for vigilant monitoring and individualized treatment strategies in populations with NSTEMI.